AI Article Synopsis
- Tissue hypoxia in solid tumors results from changes like altered blood vessel structures and tumor-related anemia, leading to decreased oxygen levels that drive tumor cells to adapt in ways that promote aggressiveness and therapy resistance.
- Induction of hypoxia inducible factors (HIFs), particularly HIF-1α, is linked to negative outcomes in breast cancer, as it encourages metastasis and makes tumors harder to treat.
- Despite efforts to target HIF-1α with small molecule inhibitors in drug-resistant breast cancers, none have succeeded in clinical applications, highlighting the need for new strategies in treatment.
Article Abstract
Tissue hypoxia in solid tumors is caused by several pathological changes associated with tumor growth, including altered microvasculature structure, increased diffusional distances, and tumor-associated anemia. As the oxygen tension decreases, tumor cells adapt to the limited oxygen supply. Previous studies have shown that such adaptation leads to an aggressive phenotype that is resistant to many anti-cancer therapies. Induction of hypoxia inducible factors (HIFs) mediates many proteomic and genomic changes associated with tumor hypoxia. In breast cancers, HIFs not only predict poor prognosis, but also promote metastasis and drug resistance. Several studies have proposed HIF-1α as a druggable target in drug-resistant breast cancers, leading to the synthesis and development of small molecule inhibitors. Disappointingly, however, none of these small molecule inhibitors have progressed to clinical use. In this review, we briefly discuss the role of HIF-1α in breast cancer drug resistance and summarize the current and future approaches to targeting this transcription factor in breast cancer treatment.
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| http://dx.doi.org/10.1016/j.canlet.2020.11.045 | DOI Listing |
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